Archive for the ‘research’ Category

Study Finds Lyme in Mouse Brains Within a Week of Infection

https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009256

A murine model of Lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system

journal.ppat.1009256.g003

Fig 3. B. burgdorferi in the dura mater are extravascular and motile.  Multiphoton image of ex vivo dura mater from C3H mouse after infection with GFP-Bb_297 for 7 days. B. burgdorferi is shown in green; collagen (second harmonics) shown in blue. Imaging parameters: Wavelength = 910 nm, pixel resolution = 135. See S1 Movie for image series movie showing spirochete motility.  https://doi.org/10.1371/journal.ppat.1009256.g003

Timothy Casselli, Ali Divan, Emilie E. Vomhof-DeKrey, Yvonne Tourand, Heidi L. Pecoraro, Catherine A. Brissette

Published: February 1, 2021

https://doi.org/10.1371/journal.ppat.1009256

 

Abstract

 

Lyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, and nervous systems including the central nervous system (CNS). Inbred laboratory mice have been used to define the kinetics of B. burgdorferi infection and host immune responses in joints and heart, however similar studies are lacking in the CNS of these animals. A tractable animal model for investigating host-Borrelia interactions in the CNS is key to understanding the mechanisms of CNS pathogenesis. Therefore, we characterized the kinetics of B. burgdorferi colonization and associated immune responses in the CNS of mice during early and subacute infection. Using fluorescence-immunohistochemistry, intravital microscopy, bacterial culture, and quantitative PCR, we found B. burgdorferi routinely colonized the dura mater of C3H mice, with peak spirochete burden at day 7 post-infection. Dura mater colonization was observed for several Lyme disease agents including B. burgdorferi, B. garinii, and B. mayonii. RNA-sequencing and quantitative RT-PCR showed that B. burgdorferi infection was associated with increased expression of inflammatory cytokines and a robust interferon (IFN) response in the dura mater. Histopathologic changes including leukocytic infiltrates and vascular changes were also observed in the meninges of infected animals. In contrast to the meninges, we did not detect B. burgdorferi, infiltrating leukocytes, or large-scale changes in cytokine profiles in the cerebral cortex or hippocampus during infection; however, both brain regions demonstrated similar changes in expression of IFN-stimulated genes as observed in peripheral tissues and meninges. Taken together, B. burgdorferi is capable of colonizing the meninges in laboratory mice, and induces localized inflammation similar to peripheral tissues. A sterile IFN response in the absence of B. burgdorferi or inflammatory cytokines is unique to the brain parenchyma, and provides insight into the potential mechanisms of CNS pathology associated with this important pathogen.

___________________

**Comment**

Technically one could say this isn’t the brain.  It’s the outer layer called the meninges – of which, the dura mater is one layer.  Regardless, this inflammation caused by infections can cause swelling, pain, and so much more.  It’s also why some Lyme/MSIDS patients have been diagnosed with Chiari.

Important excerpts:

Overall, we report that B. burgdorferi routinely colonizes the meninges in laboratory mice during early and subacute infection, and induces similar localized inflammatory gene expression profiles as other peripheral tissues as well as histopathological changes.

Conclusion:

Overall, the findings reported in this study are significant, as the lack of a tractable animal model has hindered our understanding of host-pathogen interactions in the CNS during B. burgdorferi infection. Our results provide insight into potential mechanisms of CNS pathologies associated with Lyme disease, and describe a model system that will allow for future studies evaluating the bacterial, host, and environmental factors that can contribute to the severity of CNS involvement during B. burgdorferi infection. Such studies are critical for the development and implementation of novel prophylactic and therapeutic interventions for this important disease.

The discussion section mentioned something that’s always interested me: the location of the tick bite or injection site.  The authors state that although they were able to “readily culture spirochetes from the blood of all mice at day 7 post-infection, dura spirochetes were rarely detected in mice inoculated in the footpad, and spirochete burdens were dramatically reduced in mice inoculated in the dorsal lumbar skin compared to thoracic skin.”  Further, dissemination of Bb happens in more ways than via blood and that these other ways, such as through the lymphatic system, may contribute to increased early colonization of the dura mater in mice.  This was only true for early infection and by 28 days, Bb in the dura mater were comparable regardless of the inoculation site.

This article reveals what patients have been experiencing for decades: heads that feel as if they were going to explode.  I wondered if there would ever be a day without a headache.  I personally found that Minocycline was one of the most productive antibiotics for this.  

 

 

 

Category:

Lyme, research

The Shaky Science Behind the “Deadly New Strains” of Sars-Cov-2

https://healthimpactnews.com/2021/the-shaky-science-behind-the-deadly-new-strains-of-sars-cov-2/  9-Minute Video Here

The Shaky Science Behind the “Deadly New Strains” of Sars-Cov-2

Feb. 18, 2021

by Rosemary Frei
Off-Guardian

ACCORDING TO WHAT WE HEAR FROM OFFICIALS AND THE MAINSTREAM MEDIA, THE NEW VARIANTS ARE THE MOST DANGEROUS AND UNPREDICTABLE BEINGS SINCE OSAMA BIN LADEN.

Everyone needs to stay safe from these invisible but murderously mighty microbes by shunning contact with the unwashed, unmasked and unvaccinated.

But is that drastic approach — which is accompanied by severe curtailment of civil liberties and constitutional rights — warranted?

It turns out that the case for the variants’ contagiousness and dangerousness centres largely on the theoretical effects of just one change said to stem from a mutation in the virus’s genes.

And, as I’ll show in this article, that case is very shaky.

I also have an accompanying nine-minute ‘explainer’ video (Highly recommend. Please see link at top of page)

That one change is known as N501Y — scientific shorthand for the substitution of one protein building block (amino acid) for another at position 501 in the part of the virus called the spike protein.

Specifically, position 501 lies in the portion of the spike protein that’s responsible for the intimate coupling between the virus and cells that lets the virus slip inside and multiply.

[Note that any such amino-acid switcheroo is correctly called a change, not a mutation. Mutations occur only in genes. For some reason many scientists and scribes who ought to know better are mistakenly calling N501Y and other amino-acid changes ‘mutations.’ ]

A very preliminary study published Dec. 22, 2020, suggested that N501Y also is present in the South African variant named 501Y.V2. And another very preliminary study, published January 12, 2021, asserted it was also present in the new strain emerging from the Brazilian jungle, dubbed P.1.

On top of that, the South African variant is being reported as evading immunity and B.1.1.7 sharing this escape route. And scientists are depicting new variants with N501Y on board as spreading very fast. Some say they make herd immunity impossible, so every single person on earth has to be vaccinated. The models also suggest B.1.1.7 is up to 91% deadlier than the regular novel coronavirus.

(Yet so far it seems the main basis for officials saying it’s more deadly is shown in the minutes of the Jan. 21, 2021 meeting of an influential UK committee called New and Emerging Respiratory Virus Threats Advisory Group [NERVTAG ]. There, they cite modeling papers which haven’t yet been published – which means that until they’re published there’s no way to check their work.)

THREE NON-PEER-REVIEWED THEORETICAL-MODELING PAPERS WHICH CATAPULTED VARIANTS INTO THE SPOTLIGHT

Public-health officials, politicians and the mainstream media around the world turned their collective headlights on the variants right after the publication of three theoretical-modeling papers on B.1.1.7, a variant originating in the U.K. The first was a Technical Briefing by Public Health England published Dec. 21 (it’s the first of an ongoing series of reports on the variant authored by people working at the agency and at other institutions), the second a paper published Dec. 23 by a mathematical-modeling group at the London School of Hygiene and Tropical Medicine, and the third a theoretical-modeling manuscript posted Dec. 31 by a large group of UK scientists.

None of the three papers was checked over for accuracy by objective observers – a process called ‘peer review.’ Nonetheless, all three were portrayed as solid science by many scientists, politicians, public-health officials and the press.

(I reached out for comment to Public Health England, as well as to the first author of the second paper Nicholas Davies, and to the London School of Hygiene and Tropical Medicine. The only reply I received was from a media-relations person at Public Health England; she told me no one was available for an interview.)

(Neil Ferguson was a co-author of the first and third papers. The UK government has relied on Ferguson’s mathematical modeling for many years. This is despite his work turning out to be highly inaccurate time after time. He  also supposedly stepped down from his government-advisory role last May after being caught secretly meeting with his married lover during a time when it was illegal to make contact with anyone outside of one’s household, thanks in large part to his modelling. But he was quickly restored to positions of influence. In an article and accompanying video coming out next week, I describe the connections and conflicts of interest surrounding Ferguson and the modeling papers’ other authors.)

WHAT EFFECT IS N501Y SAID TO HAVE?

In N501Y, the amino acid that’s swapped out at position 501 in the spike protein is asparagine; by scientific convention it’s represented by the letter ‘N.’ The amino acid that’s swapped in in its place is tyrosine, and it’s represented by the letter ‘Y.’ Hence ‘N501Y.’

Position 501 in the amino-acid sequence sits in the part of the spike protein that protrudes from the surface of the virus. Specifically, it’s said to lie in the region of the spike protein that latches or ‘binds’ to the mechanism that is the gatekeeper for whether the virus can enter the cell. That gate-keeping mechanism is known as the ‘ACE2 receptor.’

This region of the spike protein – known as the ‘receptor binding domain’ (RBD) — binds to the gate keeping mechanism, the ACE2 receptor. When the RBD and the ACE2 receptor bind, the cell membrane, which is the circular barrier between the area outside the cell and the cell contents, opens up and allows the virus to enter.

N501Y is posited to make the spike protein bind tighter to the ACE2 receptor. Influential theoreticians have performed mathematical modeling based on this hypothesis. This modeling suggests that this tighter binding allows the virus to enter more easily, and that therefore this makes the virus more transmissible.

Yet as far as I’ve been able to find, there is still no concrete, direct proof of this. And note that epidemiological data cannot be used to definitively detect the effect of an amino-acid in a virus. Only experiments involving direct observation of the virus’s interaction with the body can determine that.

The main evidence that the top three theoretical-models cite as proof of stronger bonding between the N501Y form of the novel coronavirus and the RBD is from just three scientific manuscripts, and these describe experiments with the virus in mice or petri dishes, not observation of whether in fact the variants are truly more contagious or more deadly.

DETAILS OF THE THREE PAPERS THAT UNDERPIN THE ASSERTION THAT N501Y BOLSTERS CONTAGIOUSNESS

One of those three papers was published Sept. 25, 2020, in Science. It describe experiments involving involving six rounds of division of the virus in mice.

The researchers found a large amount of the virus in the mice lungs right from the first round of division. Based on this, they pronounced the virus to have “enhanced infectivity.” However, they didn’t actually test whether the virus is  more transmissible/contagious – that is, whether it moves from mouse to mouse more easily.

They performed ‘deep sequencing’ and reported that they found the N501Y change in the ‘mouse-adapted’ virus. Next they did ‘structural remodeling’ on it and wrote that this analysis…

suggested that the N501Y substitution in the RBD of SARS-CoV[-2] S protein increased the binding affinity of the protein to mouse ACE2.

All of this is very different than direct observations of the variant virus’s behaviour in mice or humans.

The second paper was posted on bioRχiv on Dec. 21, 2020. It describes an “engineered decoy receptor for SARS-CoV-2.” The complicated series of molecular-biological manoeuvers in vitro were performed that is hard to follow and understand – there is no ‘Methods’ section laying out the details and sequence of what they did; rather, the researchers’ approach to their experiments is scattered across all sections of the paper including in the accompanying Supplementary Material. This is many steps removed from real-life situations. The authors conclude from their manoeuvers that laboratory-mutated novel coronavirus with the N501Y mutation seems to bind more tightly to their ‘engineered decoy’ form of the RBD receptor than the RBD receptor that normally occurs in nature.  (The idea, it seems, is that this ‘engineered decoy’ could be injected into people with the goal of getting the new variant to bind to it rather than to cells, thereby stopping it from gaining entry into cells and reproducing.)

bioRχiv is an online-only journal. (It’s pronounced ‘bioarchive’; that’s because the Greek letter χ is pronounced ‘kai.’ I presume the letter χ is used in the journal’s title because the χ2 [‘chi-square’] test is a widely used form of statistical analysis in scientific papers.) The journal has the tagline ‘The Preprint Server for Biology.’ ‘Preprint’ means non-peer-reviewed. bioRχiv focuses entirely on Covid-19-papers and is sponsored by the Chan Zuckerberg Initiative. It has a sister publication medRχiv that also focuses on Covid-19,

The Initiative is the creation of Facebook head Mark Zuckerberg and his wife Priscilla Chan. Facebook has been among the very active censors of information including scientific papers that diverge from the official narrative about Covid.

The third paper  was posted on the website of the online journal bioRχiv on June 17, 2020, and then in Cell on Sept. 3, 2020.

Like the other two papers, it is extremely removed from direct observation of the virus’s behaviour in live animals or humans. In fact, the third paper doesn’t even use human or animal cells. It involves a ‘yeast-surface-display platform’ as a basis for performing ‘deep mutational scanning’ of the novel coronavirus’s RBD. That ‘platform’ is an artificial structure the paper’s authors constructed for measuring binding between antibodies and various RBD regions containing an array of mutations.

According to this paper, the N501Y amino-acid change results in stronger binding of the virus to the RBD.

However, the papers’ authors state in the last section of their paper that:

It is important to remember that our maps define biochemical phenotypes of the RBD, not how these phenotypes relate to viral fitness. There are many complexities in the relationship between biochemical phenotypes of yeast-displayed RBD and viral fitness.

Translation: “Just because our biochemistry experiments showed that the presence of N501Y or other changes in the RBD seems to make the RBD bind tighter to the ACE2 receptor, we don’t know whether any of these changes make the virus more ‘fit’/transmissible.”

And note also that one of the authors of the third paper, Allison Greaney, is quoted as saying in an August 2020 article from the Fred Hutchison Cancer Research Center where she and several of the other authors work, that:

The virus already has a ‘good enough’ ability to bind to ACE2. There’s no reason to believe that going beyond that level will make it more pathogenic or transmissible…[b]ut the RBD may be able to tolerate a number of mutations.

As another note, the third paper was first published in bioRχiv and then published three months later in the peer-reviewed journal Cell. In Cell the paper is labelled ‘Elsevier-Sponsored Documents’ (see image below) (Elsevier is the publishing empire that owns Cell, among hundreds of other journals). I couldn’t find anything online about what ‘Sponsored’ means, nor about what or who sponsored this particular paper; and I couldn’t find any other papers with this designation. So I emailed Cell’s PR manager John Caputo on the evening of Jan. 18 and followed up by leaving him a voicemail message on Jan. 19. I haven’t heard back from him.

‘Deep Mutational Scanning of SARS-CoV-2 Receptor Binding Domain Reveals Constraints on Folding and ACE2 Binding’ (Tyler N. Starr et al.)

A BRIEF WORD ABOUT ANOTHER AMINO-ACID CHANGE IN B.1.1.7

I’ll quickly turn to another of the key changes said to be present in B.1.1.7. This change, the deletion of three amino acids was described in a paper published on the website of medRχiv on November 13, 2020. (Earlier in this article I mention that medRχiv is a creation of the Chan Zuckerberg Initiative.)

The mutation purportedly makes B.1.1.7 invisible to one of the three key functions of the polymerase chain reaction (PCR) test. That function is detection of the gene that has the genetic code for one of the two main spike proteins on the outer surface of the novel coronavirus.

However, that conclusion is based on only sequencing of the virus in a mere six people who tested positive for the novel coronavirus. On top of that, the paper was not subjected to scrutiny by other scientists (a process known as ‘peer review’) before it was published.

In addition, the Covid diagnoses of those six people were themselves determined by PCR. And PCR has been shown to have a very high rate of false positives — that is, to very frequently give a positive result in people who in fact do not harbour the novel coronavirus at all.

The authors of that paper themselves conclude that:

this result should be interpreted with caution. As a limited number of samples with the S-negative profile [i.e., tests that were positive for two of the three portions of the PCR test but not for the third, S-gene, portion] were sequenced, we could not exclude the presence of other S mutations associated with this profile…. Moreover we could not determine whether the deletion affected the primer or other probe-binding region as their coordinates were not available.

It’s a good bet that similar sleights of hand are behind the new wave of papers and headlines focusing on the amino-acid change dubbed E484K.

WHAT’S THE LESSON FROM ALL THIS?

That the pronouncements about the dire danger posed by the new variants aren’t based on solid science.

They appear to be aimed more at scaring the public into submitting to harsher and longer restrictions than helping to create truly evidence-based policies.

So follow the golden rules. Read the primary scientific-paper sources. Analyze them and think for yourself. Don’t let your reasoning be swept away by the 24-7, fear-filled news cycle.

Rosemary Frei has an MSc in molecular biology from the Faculty of Medicine at the University of Calgary, was a freelance medical writer and journalist for 22 years and now is an independent investigative journalist. You can watch her June 15 interview on The Corbett Report, read her other Off-Guardian articles follow her on Twitter and read her website here.

Category:

Activism, research, Testing, Viruses

Classification of Patients Referred Under Suspicion of Tick-borne Diseases, Copenhagen, Denmark

https://pubmed.ncbi.nlm.nih.gov/33126203/

Classification of patients referred under suspicion of tick-borne diseases, Copenhagen, Denmark

Rosa M M Gynthersen 1, Malte M Tetens 2, Mathilde Ørbæk 2, Rasmus Haahr 2, Viktoria Fana 3, Klaus Hansen 4, Helene Mens 2, Åse Bengård Andersen 2, Anne-Mette Lebech 5
Affiliations expand

Free article

Abstract

To provide better care for patients suspected of having a tick-transmitted infection, the Clinic for Tick-borne Diseases at Rigshospitalet, Copenhagen, Denmark was established. The aim of this prospective cohort study was to evaluate diagnostic outcome and to characterize demographics and clinical presentations of patients referred between the 1st of September 2017 to 31st of August 2019. A diagnosis of Lyme borreliosis was based on medical history, symptoms, serology and cerebrospinal fluid analysis. The patients were classified as:

  • definite Lyme borreliosis
  • possible Lyme borreliosis
  • post-treatment Lyme disease syndrome

Antibiotic treatment of Lyme borreliosis manifestations was initiated in accordance with the national guidelines. Patients not fulfilling the criteria of Lyme borreliosis were further investigated and discussed with an interdisciplinary team consisting of specialists from relevant specialties, according to individual clinical presentation and symptoms. Clinical information and demographics were registered and managed in a database. A total of 215 patients were included in the study period. Median age was 51 years (range 17-83 years), and 56 % were female.

Definite Lyme borreliosis was diagnosed in 45 patients, of which:

  • 20 patients had erythema migrans
  • 14 patients had definite Lyme neuroborreliosis
  • six had acrodermatitis chronica atrophicans
  • four had multiple erythema migrans
  • one had Lyme carditis
  • 12 patients were classified as possible Lyme borreliosis
  • 12 patients as post-treatment Lyme disease syndrome
A total of 146 patients (68 %) did not fulfil the diagnostic criteria of Lyme borreliosis.
  • Half of these patients (73 patients, 34 %) were diagnosed with an alternative diagnosis including inflammatory diseases, cancer diseases and two patients with a tick-associated disease other than Lyme borreliosis.

A total of 73 patients (34 %) were discharged without sign of somatic disease.

Lyme borreliosis patients had a shorter duration of symptoms prior to the first hospital encounter compared to patients discharged without a specific diagnosis (p<0.001). When comparing symptoms at presentation, patients discharged without a specific diagnosis suffered more often from general fatigue and cognitive dysfunction.

In conclusion, 66 % of all referred patients were given a specific diagnosis after ended outpatient course. A total of 32 % was diagnosed with either definite Lyme borreliosis, possible Lyme borreliosis or post-treatment Lyme disease syndrome; 34 % was diagnosed with a non-tick-associated diagnosis. Our findings underscore the complexity in diagnosing Lyme borreliosis and the importance of ruling out other diseases through careful examination.

___________________

**Comment**

While Lyme isn’t everything, it CAN BE anything.  This paper shows once again that half are turned away due to strict diagnostic criteria utilizing faulty serology testing where few are positively diagnosed. They are slapped with a label that will keep them from proper treatment and are doomed to a life of misery.

Nothing new here.  Same song, different day.

Category:

Heart Issues, Lyme, research

Experiences With Tick Exposure, Lyme Disease, and Use of Personal Prevention Methods For Tick Bites Among Members of the U.S. Population, 2013-2015

https://pubmed.ncbi.nlm.nih.gov/33217712/

Experiences with tick exposure, Lyme disease, and use of personal prevention methods for tick bites among members of the U.S. population, 2013-2015

C C Nawrocki 1, A F Hinckley 2
Affiliations expand

Abstract

Consistent and effective use of personal prevention methods for tickborne diseases, including Lyme disease (LD), is dependent on risk awareness. To improve our understanding of the general U.S. population’s experiences with tick exposure and use of personal prevention methods, we used data from ConsumerStyles, a web-based, nationally representative questionnaire on health-related topics. Questions addressed tick bites and LD diagnosis in the last year, use of personal prevention methods to prevent tick bites, and willingness to receive a theoretical LD vaccine. Of 10,551 participants surveyed over three years:

  • 12.3 % reported a tick bite for themselves or a household member in the last year, including 15.4 % of participants in high LD incidence (LDI) states, 16.3 % in states neighboring high LDI states, and 9.4 % in low LDI states.
  • Participants in high LDI states and neighboring states were most likely to use personal prevention methods, though 46.6 % of participants in high LDI states and 53.9 % in neighboring states reported not using any method. Participants in low LDI states, adults ≥ 75 years of age, those with higher incomes, and those living in urban housing tended to be less likely to practice personal prevention methods.
  • Likeliness to receive a theoretical LD vaccine was high in high LDI (64.5 %), neighboring (52.5 %), and low LDI (49.7 %) states.

Targeted educational efforts are needed to ensure those in high LDI and neighboring states, particularly older adults, are aware of their risk of LD and recommended personal prevention methods.

__________________

**Comment**

Well, well, it’s not hard to see through the veneer of this study.  Under the guise of “educational efforts,” this is nothing more than phishing to see if people will take the jab.  Our public ‘authorities’ are only concerned about Lyme disease when it suits them and typically it only suits them when there’s a lucrative vaccine in the works.  

Much has been written about the Lyme vaccine but the piece that really exposes Oz behind the curtain is this:  https://madisonarealymesupportgroup.com/2020/02/10/the-bitter-feud-over-lymerix/

For more:  https://madisonarealymesupportgroup.com/2018/01/28/the-secret-x-files-the-untold-history-of-the-lymerix-vaccine/

Excerpt:

Quotes from the patients affected by the LYMErix VACCINE:

“…..Smithkline should not be able to destroy people’s lives as they have destroyed mine …”

“… As of May 8, 2000 there were 467 adverse reactions reported to VAERS, and of them 144 had complained of some sort of joint pain. Please do not let this vaccine hurt anymore people. I know SmithKline is trying to get it approved for children, PLEASE DO NOT LET THEM HURT ANYMORE KIDS…”

“….. The FDA let them put this on the market without fully testing it. The longer that this is left on the market, the more people are going to get hurt. Please stop this madness and take it off the market…”

“….. No one else should ever suffer such profound life changes through the administration of a “safe” vaccine. He would have been far better off to get Lyme Disease than to be incapacitated by something we counted on to protect his health!…”

“….Please stop this vaccine from wrecking more lives! !Respectfully submitted…”

One thing is for certain: the Lyme vaccine has caused the very symptoms it is supposed to prohibit.  

Category:

Lyme, Prevention, research, vaccines

What Are Lyme Disease Co-Infections?

https://danielcameronmd.com/lyme-disease-co-infections/

WHAT ARE LYME DISEASE CO-INFECTIONS?

lyme disease co-infections

When Lyme disease was first discovered in 1975, it was the only known tick-borne illness recognized by clinicians. The disease, which is caused by an infection with the bacterium Borrelia burgdorferi, is transmitted through the bite of a black-legged (I. scapularis) tick.

By

Today, ticks harbor multiple infectious pathogens that can be transmitted to humans through a tick bite or tainted blood transfusion. The Centers for Disease Control and Prevention (CDC) now reports that “a single tick can transmit multiple pathogens, including bacteria, viruses, and parasites.” [1] This can result in patients developing what is referred to as Lyme disease “co-infections.”

In fact, between 2004 and 2016, the CDC identified 7 new tick-borne microbes capable of infecting humans. [1]

While most Lyme disease co-infections are acquired through the bite of an infected tick, several can be transmitted through contaminated blood transfusions. One investigation concluded, “Aside from a Babesia infection, Anaplasma is the most frequent transfusion-transmitted [tick-borne agent] with rapidly increasing clinical cases.” [2]

Ticks harbor multiple pathogens

According to a study in Suffolk County, Long Island, more than half (67%) of the ticks collected were harboring at least one pathogen. The causative agent of Lyme disease, Borrelia burgdorferi was the most prevalent (57% in adults; 27% in nymphs), followed by Babesia microti (14% in adults; 15% in nymphs).

Another study indicates that “co-infection occurs in up to 28% of black-legged ticks” in Lyme endemic areas of the United States.

Furthermore, researchers found that among infected ticks collected, 45% were co-infected and carried up to 5 different pathogens. The most prevalent co-infections included Bartonella henselae (17.6%) and Rickettsia of the spotted fever group (16.8%).

Lyme disease with co-infections

Researchers from Columbia University, Tufts Medical Center, and Yale School of Medicine examined the extent of co-infections in patients diagnosed with Lyme disease. Their findings are alarming.

  • 40% of Lyme disease patients had concurrent Babesia
  • 1 in 3 patients with Babesia had concurrent Anaplasmosis
  • Two-thirds of patients with Babesiosis experienced concurrent Lyme disease and one-third experienced concurrent Anaplasmosis
Signs and Symptoms of Lyme Disease

Recognizing and treating co-infections

As tick populations explode and expand into new geographic regions and cases of Lyme disease continue to soar, there is growing and warranted concern surrounding the medical communities’ ability to recognize, diagnose, and treat Lyme disease co-infections.

Sanchez-Vicente points out that nearly 1 in 4 black-legged ticks tested in their study had multiple infections. This finding “justifies the modification of the clinical approach to tick-borne diseases to cover all infection possibilities.”

Unfortunately, testing for co-infections rarely occurs. One study found that out of nearly 3 million specimens, only 17% were tested for non-Lyme tick-borne diseases.

Yet, an accurate diagnosis is critical, given that patients may require different treatment depending upon the type of co-infection. For instance, antibiotics prescribed for Lyme disease may be ineffective in treating parasitic or viral tick-borne diseases such as Babesia.

Most common co-infections

Lyme disease is the most common tick-borne illness in the United States. But it’s no longer the only threat. Lyme disease co-infections are becoming the norm, not the exception. The most frequently diagnosed tick-borne co-infections include Babesia, Anaplasmosis, Ehrlichia, Bartonella, Southern Tick-Associated Rash Illness (STARI), and Borrelia miyamotoi.

BABESIA

Babesia is a parasite that infects red blood cells. This parasitic infection is usually transmitted by a tick bite but can be acquired through a contaminated blood transfusion. There have also been reports of congenital transmission of Babesiosis, although rare.

Saetre describes two cases of infants with congenital babesiosis born to mothers with prepartum Lyme disease and subclinical Babesia microti infection. [3] Additionally, congenital transmission has been described in 7 previous cases, in which the infants presented with fever, anemia, and thrombocytopenia. [3]

Read more: Transfusion-transmitted Babesiosis popping up in more states in USA

Most cases of Babesia involve the strains: Babesia microti and Babesia duncani.

Symptoms typically include irregular fevers, chills, sweats, lethargy, headaches, nausea, body aches, fatigue, and in some cases, shortness of breath. But manifestations can vary.

A case series published in the Nurse Practitioner Journal demonstrates the difficulty in diagnosing the disease, as it can cause a wide range of clinical presentations.

Babesia and Lyme disease

Babesia is often present with Lyme disease and can increase the severity of Lyme disease. One study found patients co-infected with Lyme disease and Babesia experienced fatigue, headache, sweats, chills, anorexia, emotional lability, nausea, conjunctivitis, and splenomegaly more frequently than those with Lyme disease alone.

Listen to PODCAST: Delayed onset of Babesia in a Lyme disease patient

Babesia can also increase the duration of illness with Lyme disease. One study found that 50% of co-infected patients were symptomatic for 3 months or longer, compared to only 4% of patients who had Lyme disease alone.

Testing and treatment

Babesia can also be difficult to diagnose with current testing. The parasite was detected microscopically in as few as one-third of patients with Babesia. Specific amplifiable DNA and IgM antibody were more likely to be positive.

The reliability of tests for Babesia in actual practice remains to be determined.

Babesia is treated with a combination of anti-malaria medications and antibiotics such as Atovaquone with azithromycin.

EHRLICHIA

Ehrlichia is a tick-borne bacteria that infects white blood cells, but it has been found in spleen, lymph node, and kidney tissue samples. An infection with Ehrlichia can lead to Ehrlichiosis.

The infection is caused by Ehrlichia chaffeensis and Ehrlichia chagrins. The bacteria is transmitted by the Lone Star tick (Amblyomma americanum) and the black-legged tick (Ixodes scapularis).

Ehrlichia is typically transmitted by a tick bite. Only rarely, has the infection been associated with blood transfusion or organ transplant cases. According to the CDC, there have been two confirmed instances of infection occurring after kidney transplants from a common donor.

Symptoms and Treatment

Symptoms may include fatigue, fevers, headaches, and muscle aches. It can be treated with antibiotics doxycycline, minocycline, and Rifampin.

If left untreated, the disease can become severe and require hospitalization.

ANAPLASMOSIS

Anaplasmosis was previously known as Human Granulocytic Ehrlichiosis or HGE. The disease can be difficult to distinguish from Ehrlichiosis, Lyme disease, and other tick-borne illnesses.

This emerging infectious disease remains under-recognized in many areas of the United States. [4] It is caused by the bacteria Anaplasma phagocytophilum.

Anaplasmosis is spread by tick bites from the black-legged tick and western black-legged tick. Although it is reportedly rare, anaplasmosis has been transmitted through contaminated blood transfusions.

In fact, Mohan and Leiby contend that aside from a Babesia infection, “Anaplasma is the most frequent transfusion-transmitted [tick-borne agent] with rapidly increasing clinical cases.” [2]

In general, most infections with anaplasmosis are mild, “however, up to 36% of patients require hospitalization, with 3% of those having life-threatening complications.” [5]

Symptoms may include headaches, fevers, chills, malaise, and muscle aches. There have been a few reported cases describing pulmonary complications, as well. In fact, one study recommends that “anaplasmosis be included in the differential diagnosis for atypical respiratory presentations.” [5]

And although uncommon, there have been patients with anaplasmosis who did not exhibit any symptoms (asymptomatic). “It is, therefore, crucial for clinicians to be aware of potential asymptomatic anaplasmosis following a tick bite,” writes Yoo and colleagues. [6]

Anaplasmosis can be treated with antibiotics such as doxycycline, minocycline, and Rifampin.

BARTONELLA

Various Bartonella species have been found in black-legged ticks in northern New Jersey and in western black-legged ticks in California.

Bartonella can be contracted through a cat scratch or bite, causing “cat scratch fever.” But it can also be transmitted by a tick bite. In fact, “ticks and small rodents are known hosts of Bartonella and play a significant role in the preservation and circulation of Bartonella in nature.” [7]

Psychiatric presentations and other symptoms

Some patients exhibit a streak-mark rash that resembles stretch marks. Symptoms may include fever, headaches, fatigue, and swollen glands.

Several studies indicate an association between Bartonella and psychiatric symptoms. Investigators describe case studies of patients with new-onset psychiatric symptoms such as sudden agitation, panic attacks, and treatment-resistant depression possibly due to Bartonella.

Another case study highlights a young boy with a Bartonella infection who developed neuropsychiatric symptoms and was later diagnosed with pediatric acute-onset neuropsychiatric syndrome (PANS), a type of basal ganglia encephalitis. [8]

Bartonella can be treated with antibiotics such as doxycycline, minocycline, azithromycin, trimethoprim-sulfamethoxazole, clarithromycin, and Rifampin.

SOUTHERN TICK ASSOCIATED RASH ILLNESS (STARI)

STARI is an emerging tick-borne illness related to Lyme disease and was identified in the southeastern and south-central United States.

STARI is believed to be transmitted by the Lone Star tick; however, it is not officially confirmed as of yet.

The hallmark sign of STARI is an EM-like rash similar to that seen in Lyme disease. Symptoms may include fevers, headaches, stiff neck, joint pain, and fatigue.

The long term consequences and treatment of the illness have not been established.

It is not known whether antibiotic treatment is necessary or beneficial. Nevertheless, because STARI resembles early Lyme disease, physicians will often treat patients with oral antibiotics.

BORRELIA MIYAMOTOI

“B. miyamotoi is increasingly being recognized as the agent of a nonspecific febrile illness often misdiagnosed as acute Lyme disease without rash, or as ehrlichiosis.” [9]

Borrelia miyamotoi (BMD) is a spiral-shaped bacteria that causes tick-borne relapsing fevers. However, investigators point out, Borrelia miyamotoi “should not be assumed to be biologically similar to the true relapsing fever spirochetes maintained by argasid (“soft”) ticks, nor to cause typical relapsing fever.” [9]

It appears to be a common infection in areas endemic for Lyme disease. [9]

Symptoms and prevalence

A 2011 study found the disease to generally present with more systemic signs and symptoms, particularly headache and fever, compared to Lyme disease. [10]

“Virtually all patients presented with fever … fatigue, and headache …. The next most common signs and symptoms were myalgia, chills, nausea and arthralgia, characterizing 30%–60% of the patients.” [10]

Other investigators report that “patients infected with B. miyamotoi in the United States typically do not have a rash.” But they may present with “a fever in conjunction with headache (96%), myalgia (84%), arthralgia (76%), and malaise/fatigue (82%).”

READ MORE: Tiny larval ticks can transmit Borrelia miyamotoi

The prevalence of the disease is unknown but investigators report that  “studies in New England suggest that Borrelia miyamotoi infection may be as common as anaplasmosis and babesiosis.”

They also point out:

  • “Human cases are likely to be found wherever Lyme disease is endemic.”
  • “B. miyamotoi may cause serious complications, including meningoencephalitis in immunocompromised hosts.”
  • “Several studies suggest that B. miyamotoi may be transmitted through blood transfusion, consistent with the high levels of spirochetemia that occur with Borrelia species that cause relapsing fever.”

Borrelia miyamotoi is particularly concerning given that the bacterium can be transmitted to a person within the first 24 hours of tick attachment. And “the probability of transmission increases with every day an infected tick is allowed to remain attached.”

Diagnostic testing is limited. Although the CDC recommends using PCR and antibody-based tests to confirm a diagnose of B. miyamotoi, a recent study finds blood smears have poor sensitivity for confirming the disease. [9] And there is no FDA approved diagnostic test for the disease.

Treatment thus far is similar to that of Lyme disease. Studies show that doxycycline and amoxicillin have effectively treated B. miyamotoi infection in patients.

Remember, tick-borne co-infections are the norm, not the exception.

Editor’s Note: Practitioners should consider co-infections in the diagnosis when a patient’s symptoms are severe, persistent, and resistant to antibiotic therapy. Physicians have found that co-infections typically exacerbate Lyme disease symptoms.

Related Articles:

First report of malaria with Lyme disease as co-infection

Have you been bitten by a partially fed tick?

Don’t count on a relapsing fever to diagnose Borrelia miyamotoi

References:
  1. CDC Vital Signs, Weekly / May 4, 2018 / 67(17);496–501. https://www.cdc.gov/mmwr/volumes/67/wr/mm6717e1.htm
  2. Mohan KVK, Leiby DA. Emerging tick-borne diseases and blood safety: summary of a public workshop. Transfusion. 2020 Jul;60(7):1624-1632. doi: 10.1111/trf.15752. Epub 2020 Mar 24. PMID: 32208532.
  3. Kirsten Saetre, Neetu Godhwani, Mazen Maria, Darshan Patel, Guiqing Wang, Karl I Li, Gary P Wormser, Sheila M Nolan, Congenital Babesiosis After Maternal Infection With Borrelia burgdorferi and Babesia microti, Journal of the Pediatric Infectious Diseases Society, Volume 7, Issue 1, March 2018, Pages e1–e5, https://doi.org/10.1093/jpids/pix074
  4. Rocco JM, Mallarino-Haeger C, McCurry D, Shah N. Severe anaplasmosis represents a treatable cause of secondary hemophagocytic lymphohistiocytosis: Two cases and review of literature. Ticks Tick Borne Dis. 2020 Sep;11(5):101468. doi: 10.1016/j.ttbdis.2020.101468. Epub 2020 May 23. PMID: 32723647.
  5. Jose E Rivera, Katelyn Young, Tae Sung Kwon, Paula A McKenzie, Michelle A Grant, Darrell A McBride, Anaplasmosis Presenting With Respiratory Symptoms and Pneumonitis, Open Forum Infectious Diseases, Volume 7, Issue 8, August 2020, ofaa265, https://doi.org/10.1093/ofid/ofaa265
  6. Yoo J, Chung JH, Kim CM, Yun NR, Kim DM. Asymptomatic-anaplasmosis confirmation using genetic and serological tests and possible coinfection with spotted fever group Rickettsia: a case report. BMC Infect Dis. 2020;20(1):458. Published 2020 Jun 30. doi:10.1186/s12879-020-05170-9
  7. Hao L, Yuan D, Guo L, et al. Molecular detection of Bartonella in ixodid ticks collected from yaks and plateau pikas (Ochotona curzoniae) in Shiqu County, China. BMC Vet Res. 2020;16(1):235. Published 2020 Jul 9. doi:10.1186/s12917-020-02452-x
  8. Breitschwerdt EB, Greenberg R, Maggi RG, Mozayeni BR, Lewis A, Bradley JM. Bartonella henselae Bloodstream Infection in a Boy With Pediatric Acute-Onset Neuropsychiatric Syndrome. J Cent Nerv Syst Dis. 2019;11:1179573519832014. Published 2019 Mar 18. doi:10.1177/1179573519832014
  9. Telford SR, Goethert HK, Molloy PJ, Berardi V. Blood Smears Have Poor Sensitivity for Confirming Borrelia miyamotoi Disease. J Clin Microbiol. 2019 Feb 27;57(3):e01468-18. doi: 10.1128/JCM.01468-18. PMID: 30626663; PMCID: PMC6425185.
  10. Telford SR, Goethert HK, Molloy PJ, Berardi V. Blood Smears Have Poor Sensitivity for Confirming Borrelia miyamotoi Disease. J Clin Microbiol. 2019 Feb 27;57(3):e01468-18. doi: 10.1128/JCM.01468-18. PMID: 30626663; PMCID: PMC6425185.

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Category:

Anaplasmosis, Babesia, Bartonella, Borrelia Miyamotoi (Relapsing Fever Group), Lyme, research